stacks



The role of cannabinoids in adult neurogenesis


central nervous system

neuroprotection

cognition

brain injury

spinal injury

stroke

neuropathy

epilepsy

psychosis/schizophrenia

anxiety

conditioned fear

depression

amyotrophic lateral sclerosis

multiple sclerosis

Alzheimer's

Parkinson's

Tourette's


Control of the cell survival/death decision by cannabinoids.

Cannabinoids and cell fate.Conclusion: Regarding the central nervous system, most of the experimental evidence indicates that cannabinoids may protect neurons from toxic insults such as glutamaergic overstimulation, ischemia and oxidative damage.

Cannabinoids and cell fate.

Conclusion: Most of the experimental evidence indicates that cannabinoids may protect normal neurons from toxic insults.


neuroprotection

Neuroprotective antioxidants from marijuana

Conclusion: The psychotropic cannabinoid receptor agonist Δ9tetrahydrocannabinol (THC) and cannabidiol, (a non-psychoactive constituent of marijuana), both reduced NMDA, AMPA and kainate receptor mediated neurotoxicities.

Δ9-tetrahydrocannabinol protects hippocampal neurons from excitotoxicity.

Conclusion: Excitotoxic neuronal death underlies many neurodegenerative disorders. This study demonstrates the importance of agonist efficacy and the duration of treatment on the neuroprotective effects of cannabinoids.

Neuroprotective Effect of Δ9-Tetrahydrocannabinol and Cannabidiol in N-Methyl-d-Aspartate-Induced Retinal Neurotoxicity

Conclusion: In glaucoma, the increased release of glutamate is the major cause of retinal ganglion cell death. In conclusion, our results indicate that lipid peroxidation and ONOO- formation play an important role in NMDA-induced retinal neurotoxicity and cell loss in the retina, and that THC and CBD, by reducing the formation of these compounds, are effective neuroprotectants.


cognition

Neurocognition in college-aged daily marijuana users

Conclusion: Marijuana users were high functioning, demonstrating comparable IQs to controls and relatively better processing speed. Marijuana users demonstrated relative cognitive impairments in verbal memory, spatial working memory, spatial planning, and motivated decision making but comorbid use of alcohol, which was heavier in marijuana users, was unexpectedly found to be associated with better performance in some of these areas.

Is Illicit Drug Use Harmful to Cognitive Functioning in the Midadult Years?

Conclusion: At the population level, it does not appear that current illicit drug use is associated with impaired cognitive functioning in early middle age.

Effects of Smoking Marijuana on Brain Perfusion and Cognition

Smoking marijuana resulted in intoxication, as assessed by a behavioral rating scale, but did not significantly alter mean behavioral performance on the attention task. There was no significant rCBF change in the nucleus accumbens or other reward-related brain regions, nor in basal ganglia or hippocampus, which have a high density of cannabinoid receptors.

Intelligence, cognition unaffected by heavy marijuana use

Conclusion: The researchers conclude that heavy marijuana use produces no irreversible mental deficits.

Preliminary findings of a longitudinal study of effects on IQ in young adults

Conclusion: We conclude that marijuana does not have a long-term negative impact on global intelligence.

Long-term effects of marijuana use on the brain

Conclusion: Compared with controls, marijuana users had significantly less bilateral orbitofrontal gyri volume, higher functional connectivity in the orbitofrontal cortex (OFC) network, and higher structural connectivity in tracts that innervate the OFC (forceps minor) as measured by fractional anisotropy (FA)


brain injury

Cannabinoid agonist rescues learning and memory after a traumatic brain injury

Conclusion: We found that the brain-injured animals treated with the agonist showed a marked recovery.

Endocannabinoids: a new family of lipid mediators involved in the regulation of neural cell development.

Conclusion: Cannabinoids inhibit cortical neuron differentiation and promote glial differentiation. On the other hand, experiments with differentiated neurons have shown that cannabinoids also regulate neuritogenesis, axonal growth and synaptogenesis.

An endogenous cannabinoid (2-AG) is neuroprotective after brain injury.

Conclusion: When 2-AG was administered together with additional inactive 2-acyl-glycerols that are normally present in the brain, functional recovery was significantly enhanced.

Ultralow doses of cannabinoid drugs protect the mouse brain from inflammation-induced cognitive damage

Conclusion: An ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation-induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.

The effect of cannabichromene on adult neural stem/progenitor cells

Conclusion: Our results suggest that CBC raises the viability of NSPCs while inhibiting their differentiation into astroglia, possibly through up-regulation of ATP and adenosine signalling.



stimulate brain cell growth

Research Suggests Marijuana Analogue Stimulates Brain Cell Growth

Conclusion: The team found that rats treated with HU-210 on a regular basis showed neurogenesis – the growth of new brain cells in the hippocampus. This region of the brain is associated with learning and memory, as well as anxiety and depression. The effect is the opposite of most legal and illicit drugs such as alcohol, nicotine, Heroin™, and cocaine.

Effect of marijuana use on outcomes in traumatic brain injury.

Conclusion: The THC(+) group was compared with the THC(-) group with respect to injury mechanism, severity, disposition, and mortality. A positive THC screen is associated with decreased mortality in adult patients sustaining TBI.

Mechanisms of cannabidiol neuroprotection

Conclusion: Our findings demonstrate that CBD exerts robust neuroprotective effects in vivo in HI piglets, modulating excitotoxicity, oxidative stress and inflammation, and that both CB2 and 5HT1A receptors are implicated in these effects.

Neuroprotection by Δ9-Tetrahydrocannabinol against Ouabain-Induced In Vivo Excitotoxicity

Conclusion: These results provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.

The anxiolytic effect of cannabidiol on chronically stressed mice depends on hippocampal neurogenesis

Conclusion: Cannabidiol (CBD), the main non-psychotomimetic component of the plant Cannabis sativa, exerts therapeutically promising effects on human mental health such as inhibition of psychosis, anxiety and depression. However, the mechanistic bases of CBD action are unclear. Here we investigate the potential involvement of hippocampal neurogenesis in the anxiolytic effect of CBD

Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity

Conclusion: This study provides the first demonstration of CBD as an in vivo neuroprotectant and shows the efficacy of lipophilic antioxidants in preventing binge ethanol induced brain injury.




do you have a backbone?

spinal injury

Cannabinoids to treat spinal cord injury.

Conclusion: The endocannabinoid system is expressed in the intact spinal cord, and it is dramatically upregulated after lesion.

Protective effects of cannabidiol on lesion-induced intervertebral disc degeneration

Conclusion: Considering that cannabidiol presents an extremely safe profile and is currently being used clinically, these results suggest that this compound could be useful in the treatment of intervertebral disc degeneration.




stroke

Cannabinoids Can Limit Neurological Stroke Damage

Conclusion: The findings showed that the compounds could reduce the size of stroke and improve neurological function.


epilepsy

Phytocannabinoids and epilepsy

Conclusion: Phytocannabinoids produce anticonvulsant effects through the endocannabinoid system, with few adverse effects.

Analysis in conditional cannabinoid 1 receptor-knockout mice reveals neuronal subpopulation-specific effects on epileptogenesis in the kindling paradigm

Conclusion: The endocannabinoid system plays an active role in seizure termination but does not regulate epileptogenesis.


psychosis/schizophrenia

Cannabis Use and Cognition in Schizophrenia

Conclusion: Our own results confirm the overall impression from the literature review of better cognitive performance in the cannabis user group. A majority of the studies report better cognitive functioning in the cannabis-related schizophrenia and psychosis groups compared to non-drug groups.

A systematic review of the antiPsychotic properties of cannabidiol in humans.

Conclusion: The first small-scale clinical studies with CBD treatment of patients with psychotic symptoms further confirm the potential of CBD as an effective, safe and well-tolerated antiPsychotic compound

Cannabidiol enhances anandamide signaling and alleviates psychotic symptoms of schizophrenia

Conclusion: Experimental studies show that cannabidiol reduces psychosis-like effects of Δ9-tetrahydrocannabinol and synthetic analogs.

Decreased glial reactivity could be involved in the antiPsychotic-like effect of cannabidiol.

Conclusion: our data support the view that inhibition of microglial activation may improve schizophrenia symptoms.


depression

A possible role for the endocannabinoid system in the neurobiology of depression

Conclusion: Although data available are sufficient to suggest a possible involvement of the endogenous cannabinoid system in the neurobiology of depression, additional studies should be performed in order to better elucidate the role of this system in the physiopathology of depression.

Antidepressant-like effects of Δ9-tetrahydrocannabinol and rimonabant in the olfactory bulbectomised rat model of depression.

Conclusion: These findings indicate antidepressant-like behavioural properties of both THC and rimonabant in OB rats although additional studies are required to clarify the relationship between the chronic effects of cannabinoids in other pre-clinical models and in human depression.

Antidepressant-like effects of cannabidiol in mice: possible involvement of 5-HT1A receptors.

Conclusion: CBD induces antidepressant-like effects comparable to those of imipramine. These effects of CBD were probably mediated by activation of 5-HT(1A) receptors.

anxiety

Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior

Conclusion: Endocannabinoids (ECBs) such as anandamide (AEA) act by activating cannabinoid type 1 (CB1) or 2 (CB2) receptors. The anxiolytic effect of drugs that facilitate ECB effects is associated with increase in AEA levels in several encephalic areas, including the prefrontal cortex (PFC). We observed that drugs which interfere with ECB reuptake/metabolism in both the PL and in the dentate gyrus of the dHIP induced anxiolytic-like effect, in both the EPM and in the VCT via CB1 receptors, suggesting that CB1 signaling in these brain regions modulates defensive responses to both innate and learned threatening stimuli. This data further strengthens previous results indicating modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders.

Cannabinoid CB1 receptors in the dorsal hippocampus and prelimbic medial prefrontal cortex modulate anxiety-like behavior

Conclusion: Modulation of hippocampal and MPFC activity via CB1 by ECBs, which could be therapeutically targeted to treat anxiety disorders.

conditioned fear

2-AG promotes the expression of conditioned fear via cannabinoid receptor type 1 on GABAergic neurons

The cannabinoid receptor type 1 (CB1) antagonist SR141716 (3 mg/kg) caused an increase in conditioned freezing upon repeated tone presentation on three consecutive days. 2-AG fear-promoting effects depended on CB1 signaling in GABAergic neurons, while an involvement of glutamatergic neurons remained inconclusive due to the high freezing shown by vehicle-treated Glu-CB1-KO.


amyotrophic lateral sclerosis

Cannabis and amyotrophic lateral sclerosis

Conclusion: Based on the currently available scientific data, it is reasonable to think that cannabis might significantly slow the progression of ALS, potentially extending life expectancy and substantially reducing the overall burden of the disease.

Survey of cannabis use in patients with amyotrophic lateral sclerosis

Conclusion: Although the small number of people with ALS that reported using cannabis limits the interpretation of the survey findings, the results indicate that cannabis may be moderately effective at reducing symptoms of appetite loss, depression, pain, spasticity, and drooling.


multiple sclerosis

There is evidence for the use of cannabinoids for symptomatic treatment of multiple sclerosis

Conclusion: There is evidence that nabiximols oromucosal spray may reduce subjective symptoms of spasticity and that dronabinol is effective against neuropathic pain in patients with MS.

Smoked cannabis for spasticity in multiple sclerosis

Conclusion: Smoked cannabis was superior to placebo in symptom and pain reduction in participants with treatment-resistant spasticity.

Cannabinoids inhibit neurodegeneration in models of multiple sclerosis

Conclusion: Cannabinoids inhibit neurodegeneration in models of multiple sclerosis. In addition to symptom management, cannabis may also slow the neurodegenerative processes that ultimately lead to chronic disability in multiple sclerosis

Activation of Cannabinoid CB2 receptors Reduces Hyperalgesia in an Experimental Autoimmune Encephalomyelitis Mouse Model of Multiple Sclerosis

Conclusion: Our results suggest that JWH-133 acts at CB2 receptors, most likely within the dorsal horn of the spinal cord, to suppress the hypersensitivity associated with experimental autoimmune encephalomyelitis.


Parkinson's

Effects of cannabidiol in the treatment of patients with Parkinson's disease: an exploratory double-blind trial.

Conclusion: Parkinson's disease (PD) has a progressive course and is characterized by the degeneration of dopaminergic neurons. Although no neuroprotective treatments for PD have been found to date, the endocannabinoid system has emerged as a promising target. Our findings point to a possible effect of CBD in improving quality of life measures in PD patients with no psychiatric comorbidities

Cannabis (medical marijuana) treatment for motor and non-motor symptoms of Parkinson disease

Conclusion: Significant improvement of sleep and pain scores. No significant adverse effects of the drug were observed. The study suggests that cannabis might have a place in the therapeutic armamentarium of PD.

Symptom-relieving and neuroprotective effects of the phytocannabinoid Δ9-THCV

Conclusion: Given its antioxidant properties and its ability to activate CB2 but to block CB1 receptors, Δ9-THCV has a promising pharmacological profile for delaying disease progression in PD and also for ameliorating parkinsonian symptoms.

Cannabinoids provide neuroprotection against 6-hydroxydopamine toxicity

Conclusion: Our results support the view of a potential neuroprotective action of cannabinoids against the in vivo and in vitro toxicity of 6-hydroxydopamine, which might be relevant for PD. Our data indicated that these neuroprotective effects might be due, among others, to the antioxidant properties of certain plant-derived cannabinoids, or exerted through the capability of cannabinoid agonists to modulate glial function, or produced by a combination of both mechanisms.

Δ9-tetrahydrocannabinol (THC) exerts a direct neuroprotective effect in a human cell culture model of Parkinson's disease.

Conclusion: We have demonstrated up-regulation of the CB1 receptor in direct response to neuronal injury in a human PD cell culture model, and a direct neuronal protective effect of ??-THC that may be mediated through PPAR? activation.


Alzheimer's

The potential therapeutic effects of THC on Alzheimer's disease

Conclusion: These sets of data strongly suggest that THC could be a potential therapeutic treatment option for Alzheimer's disease through multiple functions and pathways.

Neuroprotection Mediated by Blockade of Microglial Activation

Conclusion: Alzheimer's disease (AD) is characterized by enhanced ß-amyloid peptide (ßA) deposition along with glial activation in senile plaques, selective neuronal loss, and cognitive deficits. Cannabinoids are neuroprotective agents against excitotoxicity in vitro and acute brain damage in vivo. Recent studies on therapeutic strategies for neurodegenerative diseases such as Parkinson's disease and AD have focused on the neuroprotective properties (e.g., slowing the ongoing neurodegeneration) rather than just on palliating symptoms of the diseases (Dawson and Dawson, 2002). Because cannabinoids combine both anti-inflammatory and neuroprotective actions, our findings may set the basis for the use of these compounds as a therapeutic approach for AD.

A Molecular Link Between the Active Component of Marijuana and Alzheimer's Disease Pathology

Conclusion: Alzheimer's disease is the leading cause of dementia among the elderly, and with the ever-increasing size of this population, cases of Alzheimer's disease are expected to triple over the next 50 years. AChE inhibitors such as THC and its analogues may provide an improved therapeutic for Alzheimer's disease, augmenting acetylcholine levels by preventing neurotransmitter degradation and reducing Aß amalgamation, thereby simultaneously treating both the symptoms and progression of Alzheimer's disease.

Prolonged oral cannabinoid administration prevents neuroinflammation, lowers ß-amyloid levels and improves cognitive performance

Conclusion: Alzheimer's disease (AD) brain shows an ongoing inflammatory condition and non-steroidal anti-inflammatories diminish the risk of suffering the neurologic disease. Cannabinoids are neuroprotective and anti-inflammatory agents with therapeutic potential. We have shown that chronically administered cannabinoid showed marked beneficial effects concomitant with inflammation reduction and increased Aß clearance.

Tourette's

Cannabinoids reduce symptoms of Tourette's syndrome

Conclusion: Currently, the treatment of Tourette's syndrome (TS) is unsatisfactory. A single-dose, cross-over study in 12 patients, as well as a 6-week, randomised trial in 24 patients, demonstrated that Δ9-tetrahydrocannabinol (THC), the most psychoactive ingredient of cannabis, reduces tics in TS patients. No serious adverse effects occurred and no impairment on neuropsychological performance was observed.





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